ARAP3 regulates neutrophil adhesion in vivo. Cremaster muscle experiments were performed on tamoxifen- and mock-induced Arap3^fl/flERT2Cre⁺ (iko) and Arap3^+/+ERT2Cre⁺ (iCre) bone marrow chimeras. Baseline levels of intravascular neutrophil adhesion (A) and neutrophil extravasation (B) were histologically evaluated in untreated, Giemsa-stained cremaster muscle whole mounts (13-17 vessels per group). (C) TNFα (500 ng intrascrotal)–stimulated neutrophil recruitment was assessed in cremaster muscle whole mounts of tamoxifen-induced Arap3^+/+ERT2Cre⁺ (22 vessels in 3 animals) and Arap3^fl/flERT2Cre⁺ mice (37 vessels in 4 mice) by quantification of intravascular and extravascular leukocytes 3 hours after injection. (D) Intravital microscopy of the TNFα-stimulated cremaster muscle was performed to assess adhesion efficiency—(adherent cells/mm²)/systemic WBC count—in postcapillary venules of tamoxifen-induced Arap3^+/+ERT2Cre⁺ (11 vessels in 3 animals) and Arap3^fl/flERT2Cre⁺ mice (18 vessels in 5 animals). (E) For evaluation of intraluminal crawling, time-lapse intravital microscopy of cremaster muscle venules (at least 3 mice per group) were recorded via CCD camera (20 frames per minute) and analyzed offline using the manual tracking plug-in of ImageJ. All data are given as means ± SEM. Data were analyzed using Kruskal-Wallis 1-way ANOVA on ranks with the Dunn post hoc test for multiple comparison or the Mann-Whitney rank-sum test for pairwise comparison. *P < .05; ** P < .01. (Detailed information on microcirculatory parameters of intravital experiments is provided in supplemental Table 1.)